Can a disrupted neuroendocrine circuit be reconstructed on an accessible surface of the brain? Having established that superior cervical ganglion (SCG) allografts become vascularized very rapidly and flourish in the IV ventricle, the next step was to see whether one of its major targets, the pineal gland, could become innervated by it and could also function. Pineal allografts have survived for at least 5 months in the IV ventricle. When transplanted to rats with their own SCG left intact, a few myelinated and unmyelinated axons penetrated the pineal graft. Like the sprouting of SCG axons in the iris, damaged during transplantations to the anterior chamber of the eye, the SCG branches to pial and choroidal vessels sent sprouts into the ventricular pineal grafts. In some ganglionectomized hosts that were given both SCG and pineal grafts, many more unmyelinated axons penetrated the grafts. These bundles of axons were ensheathed by Schwann cell processes and lay very close to capillaries and pinealocytes. The pinealocytes were identified, immunohistochemically, by their content of antigen "S" which is probably rhodopsin kinase, and electronmicroscopically, by the presence of synaptic ribbons in some of the cells. The function of the allografted pineals was considerably depressed. Urinary 6-hydroxymelatonin (6-HO-M) was undetectable by a sensitive gas chromatographic and mass spectrophotometric method in hosts that had been given a single pineal graft. It was not until 5 to 8 pineal grafts were inserted that the urinary 6-HO-M became detectable over a 24 hour collection period. In most of the recipients only about one tenth of the amount secreted by a single, intact, pineal was recovered from the urine. In 2 host rats, however, the amount--102 and 174 ng/24 hr-- was within normal limits. Thus, pineal allografts survive in the IV ventricle and become innervated by co-grafted SCG, but they function at low levels. The depressed function of the grafts may be due, in part, to the death of some pinealocytes.